Background: Numerous complications of lumbar fusion surgery have been reported, with adjacent segment disease (ASD) being one of the most important. Few studies describe the effect of sagittal, horizontal screw angles and distance of pedicle screw apex to superior endplate on the incidence of ASD in lumbar spine. The purpose of this retrospective study is to evaluate the hypothesis that unsatisfactory pedicle screw insertion positions would increase the likelihood of ASD. Methods: Outpatients with lumbar spinal stenosis underwent posterolateral lumbar fusion at L4-S1 with a least 2-year follow-up were studied. ASD at L3–L4 was defined as a condition in which intervertebral disk narrowing, posterior vertebral opening, and vertebral slippage progress at the last follow-up in comparison with the postoperative. Independent t test was performed to compare data between two groups; Spearman analysis was performed to analyze the relationship between two continuous variables. Multivariate binary logistic models were performed to identify the independent risk factors of ASD. The receiver operating characteristic (ROC) curve was performed to measure model discrimination and Hosmer–Lemeshow (H–L) test was used to measure calibration. ROC curve evaluated the discrimination ability of sagittal screw angle and distance in predicting incidence of ASD. Results: Patients in ASD group exhibit higher incidence of osteoporosis, higher Visual analogue scale (VAS), Oswestry disability index (ODI), bigger sagittal screw angle, shorter distance of pedicle screw apex to superior endplate than those in non-ASD group (p < 0.05). VAS, ODI at the last follow-up were positively correlated with Pfirrmann grade of L3–4 disk and sagittal screw angle, while negatively correlated with distance of screw apex to superior endplate (p < 0.05). Multivariate binary logistic model indicated that follow-up time (odds ratio [OR] 1.637, 95% confidence interval [CI] 1.186–2.260), distance of screw apex to superior endplate (OR 0.150, 95% CI 0.067–0.336), sagittal screw angle (OR 2.404, 95% CI 1.608–3.594) were statistically significant. The models showed great discrimination and calibration. The area under the curve of ASD identified by sagittal angle and distance was 0.895 and the cut-off values were 5.500° and 6.250 mm, respectively. Conclusion: Sagittal screw angle and distance of screw apex to superior endplate were significantly associated with the risk of ASD.

Coronavirus disease 2019 (COVID-19) is a global pandemic. Critically ill patients often require prolonged intubation for mechanical ventilation to support breathing; thus, the artificial airway must be managed by tracheotomy. Therefore, studies exploring appropriate and safe methods for tracheotomy that minimize the risks of nosocomial transmission are important. A retrospective analysis of the clinical characteristics of 14 critically ill patients with COVID-19, who underwent bedside tracheotomy from March to April 2020 was conducted to summarize the indications for tracheotomy and key points related to personal protective equipment and surgical procedures. All 14 patients were diagnosed with COVID-19 and were critically ill. All tracheotomies were performed in the late phase of the infection course. The interval between the infection and tracheotomy was 33 days, and the median interval between intubation and tracheotomy was 25.5 days. The reverse transcription-polymerase chain reaction results of secretions from the operative incision and inside the tracheotomy tube were negative. Twelve patients improved after tracheotomy, with SpO₂ levels maintained above 96%. One patient died of progressive respiratory failure; another patient died of uncontrolled septic shock. No medical staff who participated in the tracheotomy was infected. Tracheotomy in critically ill patients with COVID-19 who meet the indications for tracheotomy potentially represents a safer approach to manage the airway and help improve the treatment outcomes. A tracheotomy performed in the late phase of the disease has a relatively low risk of infection. Adherence to key steps in the tracheotomy procedure and donning adequate personal protection will help medical staff avoid infection.

Background: Apart from the current understanding of enzyme function, the mechanism of ectonucleotide pyrophosphatase/phosphodiesterase 1 (Enpp1) deficiency-associated osteoporosis is unknown. We aimed to explore the changes in the expression of signaling pathways of bone tissues involved in Enpp1 deficiency. Methods: The body weights and morphology and histology of the bones of male Enpp1 knockout (KO) and wild-type (WT) mice were assessed. The humeri of WT and Enpp1 KO mice at 12 weeks of age were subjected to high-throughput quantitative molecular measurements, and bioinformatics analysis was performed. Proteins from humeri and calvarial pre-osteoblasts (Pobs) were used to verify the differentially expressed signaling pathways and to explain the mechanism of Enpp1 deficiency-associated osteoporosis. Results: Enpp1 KO mice had significantly lower body weight and trabecular bone mass in the hindlimbs than WT mice. Proteomics and immunoblotting showed that Enpp1 deletion downregulated the expression of the p38 mitogen-activated protein kinase (MAPK) signaling pathway in bones. Lysophosphatidic acid (LPA) was involved in activating the MKK3/p38 MAPK/PCNA pathway and proliferating Pobs in Enpp1 KO mice, whereas a p38 MAPK inhibitor suppressed the LPA-induced pro-proliferation phenotype (p < 0.05). Conclusion: The inhibition of MKK3/p38 MAPK/PCNA pathway plays an important role in the development of osteoporosis caused by Enpp1 deficiency, and LPA partially rescued the proliferation of pre-osteoblasts via the MKK3/p38 MAPK/PCNA pathway.